Abstract
Complement factor 3 glomerulopathy (C3G) results from the glomerular accumulation of C3 with no accompanying immunoglobulin. Patients with C3G may have acquired factors that cause C3 dysregulation through acquired pathway, e.g. C3 nephritic factors (C3NeF), anti-complement factor H autoantibodies and/or Complement factor B autoantibodies. Two morphological and clinically distinguishable subtypes have been described and include C3 glomerulonephritis (C3GN) and dense deposit disease (DDD).
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